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somewhat arbitrarily drawn. Parasites in the limited sense act chiefly as foreign bodies, while the effect of minute vegetable organisms is rather that of ferments, in virtue of their products. Such a distinction is of relative value merely, as the micrococci and bacteria are capable of acting in other ways than by the production of septic material.

The infectious causes of inflammation are for the most part parasitic in their nature, although the discovery and identification of the parasite are in most of these inflammations assumed rather than demonstrated. The relation of the anthrax bacillus to malignant pustule no longer admits of a doubt, mainly in consequence of the researches of Koch. This investigator has been enabled to establish a definite etiological relation between the septicæmia of certain animals and accompanying minute vegetable organisms. His recent discovery of the bacillus of tuberculosis definitely removes the tubercular process from the group of dyscrasic or constitutional affections to that of the infective diseases. The constant presence of minute organisms in relapsing fever, leprosy, malaria, typhoid fever, diphtheria, erysipelas, and numerous other affections associated with, if not characterized by, inflammatory conditions, renders extremely probable the closest pathological relation between such diseases and a microscopic organism. That an inflammatory process may be regarded of infectious origin, it is necessary, according to Koch,14 that a characteristic organism should be found in all cases of the disease, and in such numbers and distribution as to account for all the phenomena of the disease in question.

14

Untersuchungen über die Aetiologie der Wundinfectionskrankheiten, 1878, 27.

These organisms may act in virtue of their growth and the consequent demand for oxygen, as seems probable in certain cases of malignant pustule, where the affected individual dies with symptoms of asphyxia. Their operation may also be like that of ferments, which produce chemical material whose effect may be remote from the immediate presence of the minute organism. They

may likewise, in connection with their colonization in various parts of the body, act more immediately upon the walls of the blood-vessels, and produce that increased porosity which is so essential a factor in inflammation.

The discovery of the immediate cause of the various infective diseases, as measles, scarlatina, variola, cholera, dysentery, mumps, whooping cough, cerebro-spinal meningitis, and numerous other epidemic and endemic affections, still remains a question for the future. The constant association of microbia with any or all of such diseases is but one fact in connection with them, and such a discovery is to be regarded merely as a step forward, to be followed by others, each of which represents not only an advance, but confirms the position attained.

The dyscrasic or constitutional causes of inflammation are those which, though long established, appear less demanded as our knowledge advances. Regarded as the result of an alteration in the composition of the blood, it is obvious that such changes may arise from the introduction, from without, of wholly foreign material. The dyscrasia may also represent modifications in the relative proportion of the normal constituents of the blood. In the former series are included what, for the most part, have already been referred to under the toxic and infectious causes of inflammation. The dyscrasiæ from lead, alcohol, and the like belong to this series. Still more important are the poisons, the virus of tuberculosis and scrofula, of leprosy and syphilis. The dyscrasiæ known as anæmia, leucæmia, uræmia, icterus, and diabetes are to be regarded less as inflammatory causes than as predisposing conditions which favor the action of other groups of causes.

The trophic causes of inflammation are those whose action is supposed to take place through the influence of nerves. Although, as has already been stated, a faulty innervation of tissues is an important element in favoring the action of various inflammatory causes, there remain certain forms of inflammation where the

disturbance of nervous action seems to be the essential feature. The occurrence of an acute peripheral gangrene soon after certain traumatic or inflammatory lesions of the brain or spinal cord, of articular inflammation following chronic affections of the cerebrospinal axis, are instances in point. The origin and distribution of herpes zoster, the occurrence of sympathetic ophthalmia and symmetrical gangrene, suggest a predominant disturbance of innervation as the exciting cause. At the same time, it is desirable to call attention to the recent observations of MacGillavray, Leber, and others,15 which suggest that a sympathetic ophthalmia is due to the extension of a septic choroiditis along the lymph-spaces of the optic nerve. It is further apparent that in certain so-called trophic inflammations, as the pneumonia after section of the pneumogastric, and the inflammation of the eye following paralysis of the trigeminus, the paralysis of the nerve is a remote, rather than an immediate cause, of the inflammation. There still remain, however, a number of localized inflammations whose origin is so intimately connected with nervous disturbances as to demand, for the present at least, a corresponding classification.

15

Wadsworth's "Report of Recent Progress in Ophthalmology," Boston Medical and

Surgical Journal, 1882, cvi. 517.

The course of an inflammation is often indicated by the predominance of certain symptoms, which, for the most part, indicate a condition of the individual acted upon rather than a peculiarity of the cause. The sthenic inflammations take place in robust individuals with powerful hearts and an abundant supply of blood. In such persons a strong pulse, high fever, and an injection of the superficial blood-vessels suggested, in former times, the necessity of bloodletting as the essential therapeutic agent. The sthenic form of inflammation was most commonly associated with pneumonia, where the obstruction to the passage of blood through the lungs was an important cause of the superficial injection of the blood-vessels.

The asthenic inflammations, on the contrary, are those occurring in feeble individuals, debilitated in consequence of pre-existing disease, exposure, or habits. A weak heart, low febrile temperature, and superficial pallor, characterize the asthenic inflammations, which show a frequent tendency to become localized in the more dependent parts of the body, the force of the circulation being too feeble to overcome the effect of gravitation.

In the typhoidal inflammations are associated those symptoms which are so prominent in the severe varieties of typhoid fever. These are the predominant symptoms: hebetude or low, muttering delirium, picking at the bed-clothes, involuntary evacuations, stertor, and the like. The nervous disturbances are associated with a feeble pulse and a dusky hue of the skin.

The constituents of an inflammatory exudation are frequently used as a basis of classification, and characterize the inflammation from the anatomical point of view. As the exudation is complex in its composition, the predominant element is made use of to designate the variety, and in doubtful cases a combined adjective indicates the presence of the two most abundant constituents. As the exudation is directly derived from the blood and contains serum in addition to white and red corpuscles, the serous, purulent, and hemorrhagic varieties of exudation naturally arise. The fibrinous and diphtheritic inflammations relate to the presence of membranes or false membranes. Finally, there are the productive inflammations, resulting in the new formation of tissue, and the destructive inflammations, where losses of substance occur.

Serous inflammations are most frequent in those parts of the body where the structure contains the largest lymph-spaces. The so-called serous cavities of the body offer the most favorable opportunities for the accumulation, as well as for the exudation, of the inflammatory product; then follow the regions of the larger lymph-spaces, according to the size and number of the latter.

The serous inflammations may also arise from the epithelial coverings of the body, as the cutaneous, alimentary, and respiratory surfaces. The serous exudations of the skin are those present in vesicles, blisters, or bullæ, which owe their limitation to the resistance offered to the spreading of the liquid inflammatory product by the coherent epidermis. Serous inflammations of the alimentary canal may assume a vesicular character, although, from the structure of its mucous membrane and the macerating influence of its contents, the vesicles are apt to be of an extremely transitory character.

The more important serous inflammations of the intestines are those manifested by profuse watery evacuations, the extreme form of which is to be found in cholera.

Serous inflammation of the lungs accompanies the more severe forms, and usually represents but a limited and circumscribed affection, associated with more abundant cellular and fibrinous products.

Serous inflammations of the peritoneum, pleura, pericardium, tunica vaginalis, and central ventricles often give rise to the presence of enormous quantities of fluid, whose partial removal from many of the cavities concerned by operative measures frequently represents a most beneficial result of treatment.

The smaller lymph-spaces of the connective tissue in various parts of the body are the frequent seat of the inflammatory oedema, so called, whose presence is an important indication of the direction assumed by a spreading inflammation, as well as a suggestion of the frequent virulence of its cause.

In general, the serous inflammations are to be regarded as less severe than other varieties, or as representing an early stage of what later may be otherwise characterized by a change in the nature of the products.

The purulent variety of inflammation is present when the exudation is abundantly cellular. As has already been stated, such cells are, for the most part, white blood-corpuscles. The purulent exudation, like the serous variety, may appear either on surfaces, when the term secretion is applied, or within the lymph-spaces of the connective tissue over a considerable space, when the pus is said to be infiltrated. When the infiltration is more circumscribed and the walls of the affected lymph-spaces are destroyed, so that adjoining cavities are thrown into larger holes, an abscess is present, from whose wall pus is constantly derived, while the inflammation is progressive.

The attention of the surgeon, in particular, has been directed to the isolation of the immediate cause of suppurative inflammation, and the modern, antiseptic, treatment of wounds is essentially based upon the view of the infectious origin of pus. The frequent presence of microbia in purulent exudation where no precautions are taken to exclude their admission, and their frequent absence or presence in minute quantities where such precautions are taken, have suggested that through their influence an inflammatory exudation is likely, if not actually compelled, to become purulent.

Whether the microbia or their products are the cause of most suppurative inflammations may be regarded as an open question. It is generally admitted, however, that, as a rule, an inflammation becomes purulent in consequence of the presence of an infective agent; in other words, that most pus is of an infectious origin and possesses infectious attributes. The labors of Lister in insisting upon the exclusion of all possible putrefactive agencies in the treatment of wounds have met with universal approval, and the basis of his treatment remains fixed, although different methods have been devised for its enforcement. His researches, and those stimulated by his work, have resulted in the establishment of principles which affect the whole field of theoretical as well as practical medicine.

Although most pus may be considered as due to the action of a virus introduced from without, and capable of indefinite progressive increase within the body, all pus is not to be regarded as of infectious origin. There are pyrogenetic agencies, like petroleum, turpentine, and croton oil, which, introduced into the body, produce suppurative inflammation without the association of microbia.

A bland pus is usually in a state of beginning putrescence, so that it is only relatively bland, and acquires extreme virulence when long exposed to putrefactive agencies. It is possible that those agencies producing an ichorous pus are the same or different from those present in bland pus. The ichorous exudation contains less corpuscles than bland pus, is more fluid, less opaque, strongly alkaline, of a greenish color, and of offensive odor.

In hemorrhagic inflammation the exudation contains large numbers of red blood-corpuscles. The occurrence of this form is sometimes associated with peculiarities of the cause, as is obvious from the epidemics of hemorrhagic small-pox, measles, scarlatina, and cerebro-spinal meningitis. It is also associated with peculiarities of the individual, as in such epidemics all cases are not equally hemorrhagic, and in scurvy the hemorrhages are attributable to the abnormal conditions to which the sufferers are exposed.

Hemorrhagic exudations are also met with in those inflammations of serous surfaces accompanying the outcropping of tubercular and cancerous or sarcomatous growths. In all cases a hemorrhagic exudation represents a grave complication, and when found in serous cavities has a certain diagnostic, as well as prognostic, importance.

Fibrinous inflammations are characterized by the presence in the exudation of considerable quantities of fibrin. As the prevailing theory of the formation of fibrin demands fibrino-plastic as well as fibrinogenous material, both are to be sought for in the exudation.

The latter is present in the liquid portion of the exudation; the existence of the former, as well as that of the ferment, is dependent

upon the presence of the white blood-corpuscles. The more numerous these, within certain limits, the more abundant the formation of fibrin. As their death appears essential for the fibrinous coagulation, the latter is most constantly met with in those parts of the body where the white blood-corpuscles are quickest separated from influences favoring their life. The farther removed they are from the blood-vessels, the more likely is their early death. Fibrinous exudations are therefore frequent and abundant in cellular and serous (sero-cellular) inflammation of the great serous cavities of the body. The clotted fibrin appears as false membrane lying upon the serous surface, either smooth or rough, tripe-like, or as villosities projecting above the surface, and again as bands, fibrinous adhesions, stretching across the cavity and uniting opposed surfaces.

The frequent occurrence of fibrinous exudations on the mucous membranes of the larynx and trachea, accompanied by the suffocative symptoms known as croup, has led to the use of the term croupous inflammation as synonymous with fibrinous inflammation, and its application to various parts of the body where croupous—i.e. suffocative—symptoms are not in question. Croupous inflammation, when used, is to be considered as an anatomical term, indicating merely the production of fibrin, and, for the avoidance of confusion, it is preferable to substitute fibrinous for croupous when such inflammations are described.

The disease, croup, it is well known, may exist without a croupous— that is, fibrinous—inflammation, as is familiarly recognized in the constant use of the terms spasmodic, membranous, and diphtheritic croup.

Fibrinous inflammation of the mucous membrane of the larger airpassages is much more frequently met with than that of mucous membranes elsewhere, as of the intestines, uterus, and bladder. The pseudo-membranous inflammations of the latter tracts are more commonly the result of the catarrhal and diphtheritic varieties than

of the fibrinous form. Fibrinous exudations on mucous surfaces, according to Weigert, can only take place when the epithelium is destroyed. Hence those causes which give rise to the destruction or detachment of the epithelium are alone capable of producing a fibrinous inflammation of mucous membranes, and a fibrinous laryngitis, trachitis, and bronchitis may result from the local application of such irritants as steam or ammonia, as well as occur in the diseases croup and diphtheria.

Fibrinous exudations may also be present within tissues, especially in those whose meshes are wide, provided the essential elements of coagulation are present. The coagulative necrosis of various organs, to be more fully mentioned hereafter, is closely allied to fibrinous clotting, the fibrino-plastic element being derived from the death of the parenchymatous cells of the part.

In the existence of a fibrinous pneumonia the conditions are somewhat analogous to those present in the fibrinous inflammation of serous surfaces and of the areolar connective tissue. There is present an abundantly cellular exudation, held in the place of its origin, the cells undergoing rapid death and surrounded by a wall whose superficial cells resemble in structure, if not in origin, the endothelial cells lining the smaller lymph-spaces of connective tissue, as well as the larger cavities within the same, known as serous cavities.

The diphtheritic inflammation is no more to be confounded with the disease diphtheria than is the fibrinous inflammation with the disease croup. Although diphtheria owes its name to the frequent presence of an apparent membrane, it may be said that the latter is not essential to the existence of the former. Diphtheria, like croup, is an affection in which various exudations may be present, and the anatomical product alone does not suffice in all instances for the recognition of the disease. In croup there may be a swollen mucous membrane, with a slight superficial mucous exudation, or a more abundant exudation of desquamated epithelium and mucus, as well

as a fibrinous false membrane. In diphtheria the same varieties of exudation may occur, and in addition the diphtheritic exudation may also be present. The latter, however, is not limited to the disease diphtheria, for its presence is apparent in other mucous membranes than that of the air-passages, and in the pharyngeal mucous membrane in other diseases than diphtheria. A diphtheritic conjunctivitis, enteritis, cystitis, and endometritis are recognized.

The cutaneous surfaces of the body may also furnish a diphtheritic exudation. The diphtheritic inflammations of wounds and of variolous eruptions are instances in point.

The characteristics of a diphtheritic inflammation are the presence within the tissues of a clotted exudation, which is associated with a defined swelling and death of the part. The exudation contains not only dead leucocytes and interlacing fibres, but is also provided with abundant granular material, much of which presents the well-known peculiarities of microscopic organisms. The apparent false membrane is thus dead, infiltrated tissue, which may be torn away from the continuous unaffected tissue, leaving a raw, rough surface, but not peeled from a comparatively smooth surface, as in other forms of pseudo-membranous inflammation.

The frequent association of a superficial false membrane, corresponding in area with that of the deeper-seated changes, in which cells and fibres may be present, is to be recognized. The diphtheritic process, however, is localized within, and not upon, the tissues affected. The diphtheritic exudation represents a local death, a necrosis, of the part concerned, and the result has frequently been compared with the death consequent upon the action of a caustic.

The immediate cause of a diphtheritic inflammation is now generally attributed to the action of microbia which enter the tissue from without, and in their growth beneath the surface produce not only the local, but also the remote, constitutional disturbances which are associated with a diphtheritic inflammation. The investigations of Wood and Formad16 point to ordinary putrefactive organisms as a

sufficient cause for the diphtheritic inflammation of diphtheria, while other observers demand a specific organism as the exciting cause.

The occurrence of diphtheritic inflammations in various parts of the body, in regions, as the intestine, where putrefactive processes are constantly present, and in the bladder and uterus, where the phenomena of putrefaction are often associated with diphtheritic inflammation, suggest the efficacy of ordinary putrefactive agencies in producing the latter. As all microbia found in putrefaction are not alike, and as the properties of certain, differ from those of others, and as our knowledge of the effects of all is but fragmentary, the characteristics of specific germs for a diphtheritic inflammation of one part of the body, or of all parts of the same, must still be regarded as not proven.

16

Research on Diphtheria for the National Board of Health, 1880, Supplement No. 7.

Productive inflammations are those which result in the new formation of tissues. One of the frequent products of inflammation is fibrous tissue, which, at first abundantly cellular, later becomes more vascular, and is finally transformed into a tissue whose fibres predominate over its cells. This formation of a cicatricial tissue demands further recognition when the termination of inflammation is considered.

In a more limited sense certain inflammations are called productive when multiple circumscribed new formations, as cancer, sarcoma, tubercle, and the like, arise in connection with the ordinary products of inflammation. Such new formations are of frequent occurrence in serous membranes, and a tuberculous pericarditis or a cancerous peritonitis, indicates that a growth of tubercles or cancerous nodules has taken place, in addition to a more or less abundant exudation with various proportions of serum fibrin and cells. This association of ordinary and transitory inflammatory products with the formation of more permanent tissues may be found within organs as well as upon surfaces. A tubercular arachnitis or lepto-meningitis presents the various products of an inflammation of the pia mater with an

abundant formation of tubercles. In like manner, a tubercular pneumonia, or a tubercular nephritis suggests an association of neoplastic growth and inflammation, in the lung and kidney. Such a relation offers a basis for the theory in favor of the inflammatory origin of tumors, and is, in part at least, a cause for the frequent consideration of tubercles as mere inflammatory products, wholly cellular or cellular and fibrous, subject to the same modifications as take place during the course of ordinary inflammations.

Even if tuberculous and scrofulous inflammations are regarded as inflammatory processes, modified by a specific cause and by peculiarities of the individual, the cancerous and sarcomatous inflammations are still to be considered as representing an association of inflammatory disturbances and specific new formations, the cause of the latter not being the cause of the former.

As ordinary inflammations of the regions concerned may take place in the absence of the neoplasms, so may the specific growth appear in the same regions without anatomical or clinical evidence of inflammation.

The classification of inflammation as to its products is supplemented by distinctions drawn with reference to the seat. The exudations may be superficial or deep-seated; they may lie within the cells, parenchyma, of an organ, or within the interstitial tissue of the same.

The product of superficial inflammations may lie on the surface, as in the case of inflamed mucous membranes, or immediately below the surface, as in numerous cutaneous inflammations, of which erysipelas may serve as the type. The term catarrhal, applied to superficial inflammations, carries with it the idea of displacement, flowing, of the exudation. The product of a catarrhal inflammation must be largely liquid, that such a displacement may readily take place, and the catarrhal exudation is chiefly composed of an excess of those elements which are present in the normal, physiological secretion from the membrane concerned. Mucus therefore

represents a frequent constituent of the catarrhal exudation, and mucous as well as muco-purulent catarrhs of the gastro-intestinal, bronchial, genito-urinary, and other mucous membranes are recognized. The catarrhal inflammation of the respective membranes usually represents the mildest form, as it demands an intact epithelium, and a ready removal of the inflammatory product.

As the cause of a catarrhal inflammation may occasion a destruction of the epithelium or a necrosis of the mucous membrane, the frequent association of catarrhal with fibrinous or diphtheritic inflammations is obvious. In such cases the clinical importance of the latter varieties gives them the precedence in the designation of the inflammation. The retention of the catarrhal products is the frequent cause of permanent disturbances of a more or less serious nature. These result in part from the mechanical obstruction offered to the function of parts beyond the seat of obstruction, as pulmonary atelectasis; and in part from the changes taking place in the retained product. Purulent otitis media with its dangerous or fatal results, and gangrene of the lung terminating in septic pleurisy, are not infrequent instances of severe disturbances from putrefaction of the retained products of a primarily catarrhal inflammation. A cheesy degeneration of the catarrhal cells leads to a surrounding fibrous, or destructive, inflammation, with a corresponding diminution in the function of the organ affected.

Of the deep-seated varieties of inflammation, that requiring special mention is the phlegmonous form. This runs its course within the less dense fibrous tissue known as the areolar or cellular tissue. The term cellulitis is usually employed by English writers to indicate the seat and nature of the process, and although the use of the term cellular tissue is rapidly becoming obsolete, the convenience of cellulitis favors the retention of the latter name.

The exudation lies within the larger lymph-spaces, and is therefore sometimes designated as the result of a lymphangitis, the deepseated, wider lymph-spaces being concerned rather than those more

superficial. Certain forms of phlegmonous inflammation are of decidedly infectious origin, and, when seated subcutaneously, are known as phlegmonous erysipelas, being thus distinguished from the simple erysipelas, whose seat is defined by the small superficial lymph-spaces of the skin.

Infective forms of cellulitis are also frequently met with in the loose, sub-peritoneal tissue of the pelvis. The infectious element usually proceeds from the uterus, and excites the malignant oedema of the broad ligament, the septic parametritis, or the pelvic cellulitis, according as the lymph-spaces inflamed lie nearer the fundus or cervix, and as the direction of the current is upward toward the spine, or outward toward the sub-peritoneal lymphatics of the pelvic wall.

Parenchymatous inflammation is present when the exudation is taken into the cells of an organ, or when the changes dependent upon inflammation of an organ take place within its functionally important cells. Virchow originally used the term parenchymatous inflammation in contradistinction to secretory inflammation, the changes in the former occurring within the elements of the tissues, while in the latter the exudation made its appearance on the surface of the organ.

Parenchymatous inflammation is manifested by a degeneration of the cells affected. This may terminate in their destruction through the conversion of their protoplasm into fat-drops, fatty degeneration; although more frequently a simple accumulation of albuminoid granules (granular degeneration) occurs. The latter represents a transitory condition, from which a return to the normal state readily takes place. This form of inflammation is met with in those organs which present a sharply-defined contrast between the functionally important cells and the connective tissue which surrounds them. The liver, kidneys, heart, spleen, pancreas, and glands in general, are consequently the most frequent seat of parenchymatous inflammation.

Opposed to this variety is the interstitial inflammation. The exudation of the latter remains within the connective-tissue framework of the organ. It is essentially cellular in character, and the number of cells is comparatively small. With their presence and the possibility of their nutrition a permanent increase in the quantity of the fibrous tissue of the organ is permitted. This becomes relatively greater in the course of time, and the parenchymatous cells become degenerated and absorbed. Interstitial inflammations are likely to become chronic in character, and, from the outset, are usually associated with parenchymatous changes.

An important clinical distinction is drawn with reference to the duration of an inflammation. Acute inflammations are those whose course is rapid, whose progress is associated with graver disturbances of function, and with a greater prominence of the cardinal symptoms. The chronic forms occupy more time in their progress, the functional disturbances, though severe, are injurious more from their protracted persistence, than their temporary violence, while redness, swelling, heat, and pain are symptoms of trifling prominence.

The exudation in acute inflammation, if recovery takes place, is rapidly removed from the place of its origin, while in the chronic variety it tends to become a part of the region in which it lies, or, if removed, slowly disappears, and may be constantly replaced. Acute inflammations may become chronic, and the chronic variety is liable to acute exacerbations.

The distinction between acute and chronic inflammations is essentially one of convenience, and, when considered from the anatomical point of view, relates rather to the persistence of the results. These may be present as a variously modified exudation or as a degenerated condition of the parenchyma of the organ or tissue affected.

Inflammation terminates in resolution, production, or destruction.

For resolution to occur it is necessary that the causes of inflammation cease to act, either by their removal or their isolation, and that their results be removed. With the removal of the results there is often associated the removal of the cause. That such may take place it is necessary that the function of the vessel walls be so restored that the exudation ceases to escape. Inflammatory products already outside the vessels, if present on surfaces with external outlets, are carried along in the course of the excretions. If they lie within the cavities of the body not opening externally, their removal is accomplished through the medium of the circulating lymph and blood, by absorption. The liquid portion of the exudation becomes a part of the circulating fluids of the body. The fibrin is converted into a granular detritus, which eventually disappears from the place of its formation. The leucocytes may return to the blood-vessels or enter the lymphatics; the latter course probably being the one taken by the larger number of the corpuscles. Many undergo a fatty degeneration, and as they lie in lymph-spaces their conversion into an emulsion permits a removal of the mechanical obstruction to the flow of lymph through the spaces in which they were accumulated.

The red blood-corpuscles are destroyed, their pigment being dissolved by the surrounding fluid and removed in the course of the circulation and excretions, or it becomes transformed into granules or crystals, which may remain in the place of their formation, or be transferred, within amoeboid cells, to remote parts of the body.

When the exudation is abundant, as in the great lymph-sacs of the body—the several serous cavities—and especially when the openings in the walls of these sacs are obstructed or the currents within them are feeble, absorption takes place with great difficulty, and demands a long interval of time. The fibrinous and cellular portion of such an exudation frequently becomes converted into a caseous mass, from a partial fatty degeneration and inspissation. This mass becomes isolated from the cavity in which it lies, usually at the most dependent portion, by the formation of a capsule of connective tissue. It may subsequently become infiltrated with lime salts,

calcified, and thus remain comparatively inert throughout the life of the individual.

The productive termination of inflammation is manifested by the new formation of connective tissue. This tissue is variously designated, as the inflammatory process is limited to the surfaces of the body exposed to the air, or the surfaces of cavities and organs, or as it lies within organs or the deep-seated parts of the body. In numerous instances it becomes a permanent constituent of the body, and, as time is usually essential for its formation, its occurrence is indicative of a chronic, rather than an acute inflammation. Certain chronic inflammations are progressive in character, the production of connective tissue being continuous, with perhaps occasional intermissions, as in the chronic interstitial inflammations of organs and tissues. The new-formed tissue, which at the outset is rich in cells, becomes in time more fibrous, and associated with this change in structure is a physical modification, manifested by its shrinkage.

This new formation may fill a gap resulting from the destruction of tissue in the progress of an inflammation, when it is present as cicatricial tissue—the scar which is usually met with upon the surfaces of the body or of certain of its organs. When opposed surfaces are united by the new-formed tissue, the term adhesion is applied; the adhesions being present as fibrous bands, cords, or membranes. The pericardial milk-spots and thickenings, the tendinous or semi-cartilaginous, indurated patches of serous membranes and of the intima of arteries, are all regarded as manifestations of a chronic inflammation of these tissues. With the localization of the inflammation in the outer walls of the bronchi and blood-vessels a thickening of the external sheath results, called a peri-bronchitis, arteritis, or phlebitis, as the case may be.

The new formation of blood-vessels is essential for the production and preservation of this connective tissue, and both arise from preexisting tissues. Pus-corpuscles represent the simple cellular product of an inflammation, and their existence is but transitory. With the new formation of blood-vessels imbedded in abundant cells there

exists a granulation-tissue, likewise transitory, but out of which arises the permanent fibrous tissue. The question is still mooted as to the part played by exuded white blood-corpuscles in the production of the permanent results of inflammation. It is generally conceded, especially since the observations of Ziegler, that they are capable of transformation into lasting constituents of tissue, into blood-vessels as well as into cells and fibres. Whether all the resulting permanent products of inflammation are dependent upon their activity, or whether the pre-existing fixed elements participate, is still to be considered undecided.

What, at present, appears most probable is, that from exuded leucocytes there arise, in the course of several days, larger cells— epithelioid or endothelioid—which are eventually associated with still larger cells, more irregular in shape, and provided with projecting filaments, giant-cells. Both varieties may result from the enlargement of leucocytes by fusion or by the assimilation of nutriment. The epithelioid cells eventually become fusiform or stellate, and their projections, as well as those of many of the giantcells, become fibrillated. The fibrils of adjoining cells, becoming united, are thus transformed into a meshwork of fibrous bundles enclosing irregular spaces, while the nuclei of the cells, with the immediately surrounding protoplasm, remain upon these bundles as the permanent cells of the new-formed tissue. The blood-vessels arise from pre-existing vessels, chiefly capillaries, and probably are also formed from the cells present in the exudation. The former method is indicated by the projection of solid sprouts from the wall of a capillary, which may unite, forming arches, and communicate with sprouts from neighboring capillaries, thus forming bridges. Both arches and bridges then become hollowed and admit the circulating blood. Ziegler maintains that the projections of the larger epithelioid cells and giant-cells become elongated, and eventually fused with capillaries, or the projections from capillaries. When this fusion is accomplished the cells become hollowed, their cavities communicating with those of the blood-vessels. These epithelioid cells, whose formation and transformation are of such importance in

the history of productive inflammation, are designated by Ziegler as formative cells, and are frequently derived from the exuded white blood-corpuscles, though not identical with them.

The inflammations not terminating in resolution or production, end in the destruction of the part. This result occurs when the nutrition of the inflamed territory is so diminished, by the changes in and around the vessels, as to become insufficient for its preservation. As the nutriment is derived through the blood-vessels, the more complete and the more permanent the stagnation in them the more likely is death to result. This event also depends upon the quantity and quality of the exudation. The more abundantly cellular the latter, the more likely is an abscess or ulcer to result.

As most abundantly cellular exudations are considered to be dependent upon the presence of putrefactive agencies, those inflammations of a predominant putrid character (gangrenous inflammations) are those terminating in destruction. The dead product is present as a slough or sequestrum, when dead soft or hard tissues are detached, entire or in part, from the living; or as a granular detritus contained in a more or less abundant liquid. The inflammatory process producing the slough and sequestrum is characterized as a gangrenous inflammation of soft parts or a caries of bone, while the process resulting in the formation of the granular detritus, and which has no necessary connection with putrefactive agencies, is called a softening, from the physical condition of its result.

Thrombosis and Embolism.

A blood-clot formed within a blood-vessel during life is called a thrombus. The entire process of which the thrombus is the essential element is designated thrombosis.

These terms were introduced by Virchow17 to avoid the confusion which resulted from regarding the process and result as synonymous with inflammation of the vessel. All writers, even at present, do not adhere to this strictness of meaning. For a thrombus of the vulva indicates a clot of extravasated blood within the connective tissue of the labium; in like manner, a vaginal thrombus is the effused and clotted blood in the loose connective tissue surrounding the vagina.

These exceptions are gradually disappearing, and the word hæmatoma, tumor composed of clotted blood, is being substituted in both instances. A cancerous thrombus represents a mass of cancerous tissue whose growth is extended along the course of a vessel, its wall having been penetrated. In general, however, the term thrombus, unless otherwise qualified, is used as first stated.

17

Handbuch der Speciellen Pathologie und Therapie, Erlangen, 1854, i. 159.

Although thrombosis is commonly a morbid process, it is not uniformly so. Its physiological significance is illustrated by the part it takes in the closure of the umbilical and uterine vessels, after childbirth. The surgeon makes use of it in his efforts to overcome certain of the ill effects of amputation, and to accomplish a cure of such local diseases as aneurism, where it is deemed important to diminish the supply of blood.

The thrombus being a blood-clot, it is composed, like the latter, of fibrin and blood-corpuscles. It is presumable that the fibrinous part of a thrombus owes its origin to the same conditions which determine the presence of fibrin in blood removed from the vessels during life or in that within the vessels after death.

According to A. Schmidt,18 the blood and other fluids, in which clotted fibrin makes its appearance, contain two generators, called fibrino-plastic and fibrinogenous. The former is considered to be paraglobulin, a substance contained mainly in the white bloodcorpuscles, while the fibrinogenous generator is held in solution in the plasma of the blood. When these materials are acted upon by a